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Exploring Health Misinformation Detection with Multi-Agent Debate
Macrophage-targeted immunocytokine leverages myeloid, T, and NK cell synergy for cancer immunotherapy
Integrative network pharmacology, transcriptomics, and microbiomics elucidate the therapeutic mechanism of <em>Polygala tenuifolia</em> Willd water extract in chronic obstructive pulmonary disease
Front Microbiol. 2025 Nov 25;16:1703853. doi: 10.3389/fmicb.2025.1703853. eCollection 2025.
ABSTRACT
BACKGROUND: Polygala tenuifolia Willd (PT) is a plant with both medicinal and edible values. Traditionally, it has been used for sedation, enhancing cognition, resolving phlegm, and relieving cough. However, its protective effects and mechanisms against chronic obstructive pulmonary disease (COPD) remain unclear.
AIM OF THE STUDY: This study aims to observe the protective effects of the water extract of Polygala tenuifolia Willd (WEPT) on COPD, and to preliminarily elucidate its potential therapeutic mechanisms by integrating network pharmacology, molecular docking, multi-omics analysis, and molecular experiments.
METHODS AND MATERIALS: HPLC quantified WEPT constituents. COPD mice models established via chronic smoke exposure underwent WEPT treatment, and the therapeutic effect was evaluated by lung function test, histopathology and cytokine profiling. Integrated multi-omics analyses (network pharmacology, transcriptomics, microbiomics) identified bioactive compounds, therapeutic targets, pathway regulations, and microbiota dynamics. Molecular docking validated compound-target interactions, while immunohistochemical/fluorescence assays confirmed key protein expression in lung tissues.
RESULTS: WEPT administration effectively reduced inflammatory cytokine levels in COPD mice, improved lung function, and alleviated histopathological damage like alveolar structural injury and airway inflammation. Network pharmacology and transcriptomic analyses identified Norhyoscyamine and Onjixanthone I as key active components, targeting PIK3CA and AKT1 via PI3K-AKT pathway regulation. Microbiome analysis showed WEPT restored gut microbiota balance. Molecular docking confirmed strong binding of bioactive compounds to core targets, while immunostaining assays demonstrated WEPT suppressed p-PI3K and p-AKT protein expression.
CONCLUSION: WEPT may exert its intervention effects on COPD through a multi-target and multi-level comprehensive regulatory mechanism.
PMID:41377050 | PMC:PMC12685879 | DOI:10.3389/fmicb.2025.1703853
AI-driven virtual cell models in preclinical research: technical pathways, validation mechanisms, and clinical translation potential
npj Digital Medicine, Published online: 11 December 2025; doi:10.1038/s41746-025-02198-6
AI-driven virtual cell models in preclinical research: technical pathways, validation mechanisms, and clinical translation potentialPotential for Algorithmic Bias in Clinical Decision Instrument Development
npj Digital Medicine, Published online: 10 December 2025; doi:10.1038/s41746-025-02119-7
Potential for Algorithmic Bias in Clinical Decision Instrument DevelopmentToward an AI Reasoning-Enabled System for Patient-Clinical Trial Matching
Beyond Traditional Diagnostics: Transforming Patient-Side Information into Predictive Insights with Knowledge Graphs and Prototypes
Multi-Agent Intelligence for Multidisciplinary Decision-Making in Gastrointestinal Oncology
Towards Foundation Models with Native Multi-Agent Intelligence
Biothreat Benchmark Generation Framework for Evaluating Frontier AI Models I: The Task-Query Architecture
ClinicalTrialsHub: Bridging Registries and Literature for Comprehensive Clinical Trial Access
Biothreat Benchmark Generation Framework for Evaluating Frontier AI Models III: Implementing the Bacterial Biothreat Benchmark (B3) Dataset
AI-powered virtual tissues from spatial proteomics for clinical diagnostics and biomedical discovery
OMNIGUARD: An Efficient Approach for AI Safety Moderation Across Languages and Modalities
Somatic evolution following cancer treatment in normal tissue
Nature, Published online: 10 December 2025; doi:10.1038/s41586-025-09792-4
High-depth sequencing of non-cancerous tissue from patients with metastatic cancer reveals single-base mutational signatures of alcohol, smoking and cancer treatments, and reveals how exogenous factors, including cancer therapies, affect somatic cell evolution.The pancreatic cancer models helping to drive innovation in the field
Nature, Published online: 10 December 2025; doi:10.1038/d41586-025-03944-2
Cellular, animal and computational models of the disease are providing fresh insights into biology and treatment.Lung Cancer Diagnosis and Prognostic Monitoring Through Cell-Free RNA via Liquid Biopsy
Ther Clin Risk Manag. 2025 Dec 2;21:1615-1636. doi: 10.2147/TCRM.S542338. eCollection 2025.
ABSTRACT
Lung cancer remains a leading cause of cancer-related mortality worldwide, largely due to challenges in its early detection and effective management. Despite advances in treatment modalities, the complex nature of lung cancer, characterized by its molecular heterogeneity and resistance mechanisms, underscores the need for innovative approaches. Cell-free RNA (cfRNA) has emerged as a promising biomarker with significant clinical applications in lung cancer diagnosis, monitoring, and precision medicine. We explore key themes including the utility of cfRNA in early detection, differentiation between benign and malignant lung nodules, molecular subtyping, and real-time therapeutic monitoring. Advances in liquid biopsy technologies, particularly non-invasive cfRNA analysis, provide dynamic means of tracking tumor evolution. cfRNA biomarkers such as miRNA, long non-coding RNAs, and circular RNAs offer unique insights into tumor biology, paving the way for personalized treatment strategies. Further, we discuss the application of cutting-edge technologies such as AI-driven analytics, next-generation sequencing, and multi-omics integration, which are enhancing the clinical utility of cfRNA in identifying treatment resistance and improving outcomes in immunotherapy, targeted therapy, and chemotherapy. The review addresses significant challenges facing cfRNA applications, including pre-analytical variability, technical limitations in detection methods, economic constraints, and the lack of standardization in clinical protocols. Through multidisciplinary collaborations and standardized methodologies, significant progress can be made toward integrating cfRNA into routine clinical practice. Emphasis is placed on future research directions, which include validating cfRNA biomarkers across diverse populations, streamlining workflows, and addressing scalability issues for real-world applications. This comprehensive exploration positions cfRNA at the forefront of innovations in lung cancer management, offering a pathway for improved diagnostic accuracy and individualized care.
PMID:41367889 | PMC:PMC12682701 | DOI:10.2147/TCRM.S542338
Decoding the enigma of multiple primary lung cancers: from mechanism to bedside-a narrative review
Transl Lung Cancer Res. 2025 Nov 30;14(11):5181-5197. doi: 10.21037/tlcr-2025-957. Epub 2025 Nov 27.
ABSTRACT
BACKGROUND AND OBJECTIVE: Lung cancer is the leading cause of global cancer mortality. Multiple primary lung cancer (MPLC) represents a clinically challenging subtype characterized by independent tumor foci. Distinguishing MPLC from intrapulmonary metastases is crucial for prognosis and treatment. This review integrates current evidence on MPLC's etiology, molecular mechanisms, diagnosis, and management, aiming to provide a clinical reference and highlight future precision medicine directions.
METHODS: We searched PubMed/MEDLINE, Web of Science, and Google Scholar for articles published between January 2000 and September 2024. Search terms included "multiple primary lung cancer", "diagnosis", "molecular characteristics", and "treatment". The selection focused on English-language research and reviews addressing MPLC pathogenesis, diagnosis, or management.
KEY CONTENT AND FINDINGS: The review delineates the multifactorial pathogenesis of MPLC, encompassing genetic susceptibility, somatic heterogeneity, clonal evolution, and epigenetic dysregulation. It frames these mechanisms against a backdrop of "field cancerization" and dynamic tumor microenvironment interactions. The evolution of diagnosis from histology to integrated molecular-artificial intelligence (AI) models is detailed, alongside treatment strategies that must overcome the challenge of inter-lesional heterogeneity.
CONCLUSIONS: MPLC is a distinct entity arising from genetic, epigenetic, and microenvironmental interplay. Advancing its management requires multi-omics integration to decipher pathology and identify biomarkers. Future work should develop AI-enhanced diagnostics and lesion-specific treatment strategies. This review synthesizes current evidence to inform and direct future research and clinical innovation in MPLC.
PMID:41367572 | PMC:PMC12683420 | DOI:10.21037/tlcr-2025-957
Causal relationship of immune cell characteristics in hepatocellular carcinoma: A multi-omics analysis based on Mendelian randomization
Medicine (Baltimore). 2025 Dec 5;104(49):e45942. doi: 10.1097/MD.0000000000045942.
ABSTRACT
The tumor immune microenvironment of hepatocellular carcinoma (HCC) is complex, yet the causal relationship between immune cell subpopulations and HCC risk remains incompletely elucidated. This study aims to systematically evaluate the causal association between immune cell subpopulations and HCC using Mendelian randomization (MR) analysis, and to validate the biological mechanisms underlying these associations through multi-omics data. Bidirectional two-sample MR analysis was performed to examine causal relationships between 731 immune cell subpopulations and HCC. Inverse-variance weighting (IVW) served as the primary analysis method, with robustness validation through Bayesian weighted MR (BWMR) and machine learning algorithms. Therefore, for significantly associated immune subpopulations, independent analyses of gene expression, prognosis, and tumor immune microenvironment were conducted using HCC data from the Cancer Genome Atlas (TCGA) LIHC cohort. MR analysis and validation identified 21 immune cell subpopulations with significant causal associations to HCC risk. Among these, 12 were identified as risk factors, and 9 as protective factors. Validation in the TCGA cohort revealed that risk-associated immune subpopulations were predominantly enriched for markers of T cell exhaustion and immunosuppressive microenvironments, whereas protective subpopulations likely represented a distinct regulatory B cell subset whose function was associated with the anti-inflammatory factor interleukin-10. This study genetically confirms that specific immune cell functional subpopulations constitute causal risk factors for HCC. These subpopulations exert their effects by shaping distinct tumor immune microenvironments. These findings provide novel mechanisms for understanding the immunopathogenesis of HCC and identify potential targets for developing novel immune intervention strategies.
PMID:41366997 | DOI:10.1097/MD.0000000000045942